Expression and clinical significance of CCN5 and the oestrogen receptor in advanced breast cancer

Abstract Purpose The aim of this study was to investigate the expression and clinical implications of CCN family member 5 (CCN5) and the oestrogen receptor (ER) in advanced breast cancer (BC). Methods A total of 130 patients with advanced BC were selected for the study. Samples of normal breast tissue, ductal carcinoma in situ (DCIS), and invasive carcinoma were collected. The expression levels of CCN5 and ER in these tissues were examined using immunohistochemical methods. The correlation between expression of CCN5 and ER in different tissues and also differences in expression in invasive carcinoma were analysed. In addition, the relationship between CCN5 expression in advanced BC tissues and clinical pathological features was examined. Results CCN5 and ER had low expression in normal breast tissues and invasive carcinoma tissues, but high expression in DCIS, with this difference being statistically significant (X 2 = 119.899, P < 0.001; X 2 = 113.524, P < 0.001, respectively). The expression of CCN5 and ER in different tissues of patients with advanced BC showed a positive correlation. Significant differences were also observed in the positive and negative expression of CCN5 and ER (X 2 = 56.358, P < 0.001). Moreover, the expression of CCN5 protein in advanced BC showed a statistically significant associations ( P < 0.05) with the expression of the progesterone receptor (PR), human epidermal growth factor receptor 2 (HER-2), Ki-67, and P53, tumor diameter, histological grade, lymph node metastasis, pathological molecular subtype, and clinical staging. Conclusion High expression of CCN5 and ER was observed in DCIS tissues of patients with advanced BC, with their expression being positively correlated. These findings suggest that CCN5 and ER may have a potential synergistic role in the progression of BC that influences the progression of advanced BC and can also be used to predict the effectiveness of endocrine therapy.